The proposed study will investigate the complicated pathogenesis of early experimental cerebral edema, induced by cold lesions through the intact dura. Quantitative studies of the status of acid-base metabolism, and energy metabolism, in brain tissue frozen in situ will be undertaken. These will consist of the status of brain regulation of H plus activity, as shown by the CO2 buffer capacity, and osidative metabolism evaluated from redox potentials. In addition, lactate, pyruvate, labile phosphates will be measured. Regional cerebral blood flow will be measured by the C-14 antipyrine method. Interrelationships of such regional metabolic parameters with regional cerebral blood flow and vascular reactivity in early cerebral edema will be studied. The effect of alterations of paCO2 and of alterations in systemic blood pressure on cerebral blood flow (autoregulation) will also be studied. Therapeutic modalities in cerebral edema consisting of corticosteroids, glycerol, and prolonged hyperventilation, will be investigated with regard to their effects on the parameters described above.